Deficiency of Vitamin A in body. Vitamin A deficiency is most common in Africa and Southeast Asia. Vitamin A deficiency can cause blindness. It can also increase the risk of serious, sometimes fatal, infections. Symptoms include night blindness, dry skin and frequent infections.

1. Causes, Clinical Features, Treatment and Prognosis in
Vitamin A Deficiency
&
Emphasis on Preventable Causes and Prophylactic
Measures
Dr. Sarjil Amin

2. Vitamin A
● Vitamins are class of organic compounds categorized as essential
micronutrients in which Vitamin A is FAT SOLUBLE VITAMIN along with
Vitamins D, E & K.
● Vitamin A consist of Retinol (Preformed Vitamin), Retinal, Retinoic Acid & β-
Carotene (Pro-Vitamin).
● Essential for
○ Immunity
○ Growth
○ Cell Differentiation
○ Reproduction
○ VISION

3. Sources
● Liver
● Fish Liver Oil
● Butter
● Eggs & Meat
● Milk
● Cheese
● Green Vegetables
○ Spinach, Carrots,
○ Green & Yellow Fruits

4. Metabolism
● Liver stores 90% of Vitamin A as Retinol Palmitate
● Active Metabolites
○ Trans-Retinoic Acid
○ Cis-Retinoic Acid
● Regulate Expression of Keratins & Mucins
● Rhodopsin in Visual Cycle

5. Vitamin A Deficiency Factors
● ↓ed Intake
● Impaired Absorption
● Alteted Storage
● ↑ed Utilization
● Chronic Diarrhea
● Malabsorption
Ocular manifestations of Vitamin A Deficiency are referred as XEROPHTHALMIA

6. Deficiency - WHO Statistics
● An estimated 250 million preschool children are vitamin A deficient and it is
likely that in vitamin A deficient areas a substantial proportion of pregnant
women is vitamin A deficient.
● An estimated 250 000 to 500 000 vitamin A deficient children become BLIND
EVERY YEAR, half of them DYING within 12 months of losing their sight.

7. Vitamin A Deficiency - WHO Classification
● Night blindness (XN)
● Conjunctival xerosis (X1A)
● Bitot's spots (X1B)
● Corneal xerosis (X2)
● Corneal ulcer covering less than 1/3 of the cornea (X3A)
● Corneal ulcer covering at least 1/3 of the cornea, defined as keratomalacia
(X3B)
● Corneal scarring (XS)

8. Night blindness - XN
● Earliest symptom
● Inability to see in dim light
● Occurs due to impairment in DARK ADAPTATION
● Vitamin A Level < 0.70 MMol/Lit.

9. Conjunctivital Xerosis - X1A
● First Sign of Vitamin A deficiency
● Conjunctiva becomes dry & non-wettable
● Patches seen in interpalpebral of the nasal & temporal quadrants
● In advance cases it involves the whole conjunctiva resulting in Conjunctival
Thickening & Wrinkling instead of normal shiny-smooth conjunctiva.

10. Bitot’s Spot - X1B
● They are triangular, pearly white or yellowish, foamy spots on the BULBAR
CONJUCTIVA on either side of the CORNEA.
● Usually bilateral
● In YOUNG children, it indicates Vit.A deficiency
● In OLDER individuals, it is often an inactive sequelae of earlier disease.

11. Corneal Xerosis - X2
● Punctate Keratopathy - The cornea appears dull, dry and non-wettable and
eventually opaque.
● Nasally
● Granular pebby dryness
● Cornea lacks lustre
● In more SEVERE DEFICIENCY, there maybe X2 → X3 (Corneal Ulceration).
● The ulcer may heal leaving a corneal scar which may affect vision.

12. X2 - Corneal Xerosis

13. Keratomalacia - X3A & X3B
● It is the liquefaction of the cornea. This is an MEDICAL EMERGENCY.
● The cornea(a part or the whole) may become soft and may burst open.
● Due to liquefactive necrosis
○ Small ulcers in peripheral
○ Large ulcers involve centrally or entire cornea
● This process is rapid and if the eye collapses then vision is lost (Blindness).

14. Corneal Scarring - XS
● Healing of stromal defects results in corneal scar of different densities and
size which affects vision.

16. Extra Ocular Manifestations
● Follicular Hyperkeratosis
● Anorexia
● Growth Retardation

17. Treatment
● DIRECT
○ SUPELIMENTATION
○ FORTIFICATION
● INDIRECT
○ PUBLIC HEALTH MEASURES TO CONTROL DISEASES
● Vit. A deficiency should be treated urgently
● Nearly ALL the early stages of Xeropthalmia can be REVERSED by:
● Administration of MASSIVE DOSE of 2,00,000 IU (or 110mg) of retinol palmitate ORALLY on
2 successive days.
● ALL children with corneal ulcers are given Vit. A whether or not a deficiency is suspected.

21. Prevention & Control
● Short Term
○ Administration of Large doses of Vitamin A
● Medium Term
○ Fortifications of Food
● Long Term
○ Reduction & Elimination of Factors contributing to Ocular Diseases

22. Short Term Actions
● A simple technology was developed by the National Institute of Nutrition
(Hyderabad).
● The strategy is to administer SINGLE MASSIVE DOSE of Vit. A in oil(retinol
palmitate) ORALLY.

23. Medium Term Actions
● FORTIFICATION of certain food [such as dalda(vanaspati), margarine & dried
skimmed milk] with Vitamin A.
● Fortification is successful only if the chosen food is consumed in sufficient
quantities by groups at risk.

24. Long Term Actions
● REDUCING or ELIMINATING the frequency and severity of contributory
factors to ocular disease (PEM, respiratory tract infections, diarrhoea,
measles)-
○ To consume green leafy vegetables or other Vit. A rich food
○ Promotion of breast feeding
○ Improvements in environmental health (such as ensuring safe and adequate WATER
SUPPLY, maintenance of SANITARY LATRINES to safeguard against diarrhoea)
○ Immunization against infectious diseases (measles), prompt treatment of diarrhoea and other
infections
○ Better feeding of infants and young children
○ Improved health services for mothers and children
○ Social and health education.

25. Assessment of Vitamin A Deficiency
● It is done by population surveys employing both CLINICAL and
BIOCHEMICAL criteria.
● The surveys are done on pre-school children (6months to 6years) based on
prevalence criteria.
● Presence of any one of the criteria should be considered as EVIDENCE of a
xeropthalmia problem in the community.

28. ● Cure was associated with certain foods in early times with topical application or ingestion of
animal and fish liver, and in later years with ingestion of plant foods containing green and
yellow pigments (Wolf, 1996).
● Steenbock (1919) postulated, and later confirmed, that carotenoid from yellow maize (com)
could support growth and prevent ocular lesions. Since Isler et al. (1947) discovered a cost-
effective way to synthesize vitamin A, cure and prevention are also possible through
commercially produced, synthetic vitamin A.
● Breast-fed infants do not usually show clinical deficiency for at least 4 to 6 months after birth.
They may be at a marginally adequate point however, if breast-fed by a malnourished vitamin
A-depleted mother (Underwood, 1994a)
● At the same time, if breast-fed, even from a mainourished mother whose breast milk vitamin
A has been improved through direct matemal supplementation (200,000 IU of vitamin A given
within 2 months postpartum (WHO/UNICEF/IVACG, in press), adequate infant vitamin A
status may be prolonged beyond 6 months (Stoltzius et al. 1993).
Research

29. Research
● Vitamin A requirements, therefore, are greatest during periods of rapid growth-
infancy and early childhood, adolescence, and pregnancy-and when the vitamin is
lost from the body through normal physiologic processes, such as lactation, or
through nonphysiological losses brought about by frequent disease, such as
malabsorption, diarrhea, and febrile. infections (FAO/WHO, 1988).
● The bioavailability of the provitamin A carotenoids from plants is greatly influenced
by the nature of the embedding matrix (.e, fibrous, dark green leafy vegetables
[DGLV] or soft-fleshed yellow/orange vegetables and fruits) and the composition
of the accompanying meal.
● Populations with subclinical deficiency-tissue concentrations of vitamin A low
enough to have adverse health consequences, even in the absence of
xerophthalmia, WHO's current definition of VAD (WHO, 1996a).

30. Approaches To The Prevention or Correction Of VAD
● Vitamin A intervention approaches are commonly grouped into two main control
strategies: (1) direct increase in vitamin A intake through dietary modification with
natural or fortified foods and supplements and (2) indirect public health measures
to control disease frequency. Information, education, and communication (IEC),
including social marketing and specific vitamin A-oriented nutrition education, may
or may not accompany each of the above interventions.
● VAD-endemic areas require special attention to micronutrient supplementation.
● Vitamin A plays a central role in the body's ability to fight off infectious diseases,
deficiency can have far-reaching health consequences. People with a Vitamin A
deficiency are more susceptible to measles, diarrhoea, respiratory infections and
HIV/AIDS.

31. ● Improving the vitamin A status of deficient children aged 6 months to 6 years dramatically
increases their chances of survival.
● Good vitamin A status is associated with reduction in the rate of hospital admissions and
reduced need for out-patient services at clinics and therefore lowers overall cost of health
services.
● Recent studies suggest that preventing vitamin A deficiency of women during and before
pregnancy greatly reduces their risk of mortality and morbidity around the time of childbirth,
probably through increasing resistance to infection and lowering levels of anaemia.
● Many International organizations like UNICEF and WHO have made the strategies for the
prevention and elimination of vitamin A deficiency disease and they provide these strategies
to the affected countries in the form of action plan, literature
● It is the responsibility of the governments and the health departments of the affected
countries to implement these strategies for the betterment of the future of common people
and children.
Approaches To The Prevention or Correction Of VAD

32. Vitamin A Toxicity
● An EXCESS intake of RETINOL causes nausea, vomiting, anorexia and
sleep disorders followed by skin desquamation and then enlarged liver and
papillar oedema.
● HIGH intakes of CAROTENE may colour plasma and skin.

33. Thank You !!!